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Orthogonal engineering of adoptively transferred CD8+ T cells to co-express two cytokines — an IL-2Rβ/γ-biased IL-2 variant and the proinflammatory alarmin IL-33 — induces an exhaustion-resistant synthetic cell state with potent anti-tumor efficacy in the absence of host pre-conditioning.
APLAID is a very rare autoinflammatory disease thought to be caused by mutations in PLCG2. A mouse model of APLAID recapitulates clinical features of the disease, and identifies a crucial function for G-CSF that might be targeted therapeutically.
The immune system is not immune to sex differences. New research now uncovers the molecular mechanisms that underlie sex-based differences during antiviral immune responses.
Mononuclear phagocyte proliferation is thought to be limited to myeloid progenitor cells and mature macrophages. However, availability within an interstitial macrophage niche permits the proliferation of monocytes in the lung before macrophage differentiation.
Capturing cell organization in the tumor microenvironment using spatial proteomics can provide insight into the disease. A pair of studies applying this to advanced lung and brain tumors identifies organizational immune hallmarks that are associated with patient outcomes.
Antibody dynamics resulting from sequential immunization are complex, limiting the study of concepts such as ‘original antigenic sin’. Here, molecular fate-mapping defines an ‘addiction’ of boosted antibodies to primary clones, and OAS-like suppression of new clones, to a degree inversely related to boosting antigenic distance.
Taking advantage of intersectional genetics, Valente et al. report a novel strategy for tracking plasmacytoid dendritic cells (DCs) that enables their discrimination from conventional DCs and plasmacytoid DC–like cells, as well as transitional DCs.
The NLRP10 protein is found to form an inflammasome complex in response to mitochondrial damage. Loss of NLRP10 from colonic epithelia promotes inflammatory bowel disease in a mouse model, while a variant predisposing to atopic dermatitis also shows loss of function.
Several panels of naturally arising antibodies against specific chemokines are closely correlated with various favorable COVID-19 outcomes, raising an opportunity to target the chemokine system for long COVID treatment.
A serendipitous behavioral observation in a mouse line led to the discovery that macrophages modulate acute pain. The macrophage-derived protein SNX25 sets the threshold for acute pain through tonic NGF signaling to cutaneous sensory neurons.
Research shows that Vδ1 and Vδ3 γδ T cells that express PD-1 and display potent cytotoxic functions are key immune responders in HLA-class-I-negative colon cancers subjected to immune checkpoint blockade therapy.
In addition to the acute phase of SARS-CoV-2 infection, a significant percentage of patients experience a prolonged illness with varying symptomatology. Longitudinal SARS-CoV-2 patient-centric immunologic, inflammatory and metabolic data collection has allowed the generation of a composite signature to predict recovery.
TH17 cells combat infection but can also drive pathological inflammation. A TH17 cell NLRP3–caspase-8–caspase-3–GSDME axis is now shown to release the alarmin IL-1α without triggering cell death.
Human resident memory T (TRM) cells clonally segregate in distinct tissues, with gene expression signatures tailored to those sites. Hence, beyond a shared language of residency, TRM cells may acquire local dialects to provide site-specific immunity.
A specialized subset of iNKT cells populates the skin in early life, where their supply of transferrin regulates iron metabolism to promote hair follicle development.
Signaling via T cell antigen receptors is diminished during aging. But paradoxically, CD4+ T cells from older adults tend to differentiate into effector-like rather than memory cells. An altered balance between the activities of HELIOS, IL-2Rα, and STAT5 influences this decision.
Expression of the inhibitory receptor PD-1 on regulatory T cells in the tumor microenvironment provides intrinsic stabilization, proliferation and metabolic rewiring signals to restrain tumor immunity.
Diverse inflammasome stimuli recruit NLRP3 to dysfunctional endosomes via interactions with lipids that accumulate in excess on these organelles. Excess lipid detection may be a common principle that explains NLRP3 function in health and disease.
